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Cell Immunol. 2016 Dec;310:141-149. doi: 10.1016/j.cellimm.2016.08.015. Epub 2016 Sep 4.

Significant role for IRF3 in both T cell and APC effector functions during T cell responses.

Author information

1
School of Biological Sciences, University of Nebraska-Lincoln, United States.
2
School of Biological Sciences, University of Nebraska-Lincoln, United States; Nebraska Center for Virology, University of Nebraska-Lincoln, United States.
3
Nebraska Center for Virology, University of Nebraska-Lincoln, United States; Department of Oral Biology, University of Nebraska Medical Center, Lincoln, NE, United States. Electronic address: tpetro@unmc.edu.

Abstract

Interferon Regulatory Factor (IRF)3 is a crucial transcription factor during innate immune responses. Here we show IRF3 also has a role in adaptive T cell immune responses. Expression of IFN-γ, IL-17, and Granzyme B (GrB) during in vitro T cell responses was impaired when either dendritic cells (DCs) or T cells were derived from IRF3KO mice. Unexpectedly, IRF3-dependent NK-activating molecule (INAM), which is an NK cell activating factor of the DC innate immune response, was induced during the T cell response. Additionally, supernatants from responding T cells induced ISG54 in the RAW264.7 macrophage cell line in an IRF3 dependent manner. Moreover, addition of anti-IFN-γ prevented supernatant induction of ISG54 and recombinant IFN-γ stimulated ISG54 expression. Thus, IRF3 in APCs and T cells is required for optimal T-cell effector function and the ability of T cells to influence innate immune function of APCs.

KEYWORDS:

Dendritic cells; Granzyme-B; Innate immunity; Interferon Regulatory Factor-3; Interferon stimulated gene-54; Interferon-γ; Interleukin-17; T cells

PMID:
27641636
PMCID:
PMC5125847
DOI:
10.1016/j.cellimm.2016.08.015
[Indexed for MEDLINE]
Free PMC Article

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